Month: December 2016

The American Psychological Association article, Controlling anger before it controls you, continued. A lecture on how incompetent, and defective and hopeless you are (Original Sin).

Is It Good To “Let it All Hang Out?”

Psychologists(those handy elves again – what a convenient crutch for not supplying any evidence!) now say that this is a dangerous myth. (So, it’s a myth that psychs used to support? What a damning admission! LOL) Some people use this theory (“letting it all hang out” is not a theory) as a license to hurt others. Research has found that “letting it rip” with anger actually escalates anger and aggression and does nothing to help you (or the person you’re angry with) resolve the situation.

Strategies to keep anger at bay (again – this “thing” that lives like a parasite in your brain – ridiculous and defeatist)

It’s best to find out what it is that triggers your anger, and then to develop strategies (but to save time, we will dictate what “solutions” we approve for you) to keep those triggers from tipping you over the edge.

Relaxation

Simple relaxation tools, such as deep breathing and relaxing imagery, can help calm down angry feelings. There are books and courses that can teach you relaxation techniques, and once you learn the techniques, you can call upon them in any situation. If you are involved in a relationship where both partners are hot-tempered, it might be a good idea for both of you to learn these techniques.

Slowly repeat a calm word or phrase such as “relax,” “take it easy.” Repeat it to yourself while breathing deeply.

Use imagery; visualize a relaxing experience, from either your memory or your imagination.

Nonstrenuous, slow yoga-like exercises can relax your muscles and make you feel much calmer.

Practice these techniques daily. Learn to use them automatically when you’re in a tense situation. (Yes! When you are in a domestic argument, stop and do some yoga-like exercises before grabbing your gun; take a deep breath (your aim will be better), and then shoot. Note that none of these instructions address anger, nor solve the situation; they are, in fact, negative adaptions meant to control “feelings” temporarily, but subject the angry person, and the object of their anger, to ongoing unresolved stress.)

Cognitive Restructuring

Simply put, this means changing the way you think. Angry people tend to curse, swear, or speak in highly colorful terms that reflect their inner thoughts. When you’re angry, your thinking can get very exaggerated and overly dramatic. Try replacing these thoughts with more rational ones. For instance, instead of telling yourself, “oh, it’s awful, it’s terrible, everything’s ruined,” tell yourself, “it’s frustrating, and it’s understandable that I’m upset about it, but it’s not the end of the world and getting angry is not going to fix it anyhow.”

Be careful of words like “never” or “always” when talking about yourself or someone else. “This !&*%@ machine never works,” or “you’re always forgetting things” are not just inaccurate, they also serve to make you feel that your anger is justified and that there’s no way to solve the problem. (This is the conclusion toward which the reader is being manipulated.) They also alienate and humiliate people who might otherwise be willing to work with you on a solution. (It is also possible that the source of anger IS the people who are UNWILLING to work with you toward a solution, even if it’s specified in their job description or marriage vow.)

Remind yourself that getting angry is not going to fix anything, that it won’t make you feel better (and may actually make you feel worse).

Logic defeats anger(as a logical thinker, I find this assertion to be ridiculous -) because anger, even when it’s justified, can quickly become irrational. So use cold hard logic on yourself:(Note; the following “advice” is not logic – it’s rationalization for why you are a “bad person”) Remind yourself that the world is “not out to get you,” (but specific people may be!) you’re just experiencing some of the rough spots of daily life. Do this each time you feel anger getting the best of you, and it’ll help you get a more balanced (and unrealistic)perspective.

Angry people tend to demand things: fairness, appreciation, agreement,willingness to do things their way. (OMG! if this doesn’t tip you off as to what’s going on, NOTHING WILL! “Fairness, appreciation for your efforts and accomplishments – and workable agreements” are what you ought to expect from other people – but these “normal” expectations are paired with BEING SELFISH.)

Everyone wants these things, and we are all hurt and disappointed when we don’t get them, but angry peopledemand them ( Or…people perhaps, who simply want justice, fairness and honesty in their “human environment”. This “shaming” is so typical and is used against – let’s say – Black Americans who (are forced to) demand rights in practice, which are ALREADY THEIRS BY LAW as American citizens), and when their demands aren’t met, their disappointment becomes anger. As part of their cognitive restructuring, angry people need to become aware of their demanding nature and translate their expectations into desires. In other words, saying, “I would like” something is healthier than saying, “I demand” or “I must have” something. When you’re unable to get what you want, you will experience the normal reactions—frustration, disappointment, hurt—but not anger. Some angry people use this anger as a way to avoid feeling hurt, but that doesn’t mean the hurt goes away. (Negative adaptations are social demands that require individuals to “put up with” unhealthy environments.)

Do you need counseling? Here we go! Salvation for your sins…

If you feel that your anger is really out of control, if it is having an impact on your relationships and on important parts of your life, you might consider counseling to learn how to handle it better. A psychologist or other licensed mental health professional can work with you in developing a range of techniques for changing your thinking and your behavior.

When you talk to a prospective therapist, tell her or him that you have problems with anger that you want to work on, and ask about his or her approach to anger management. Make sure this isn’t only a course of action designed to “put you in touch with your feelings and express them”—that may be precisely what your problem is. With counseling, psychologists say, a highly angry person can move closer to a middle range of anger in about 8 to 10 weeks, depending on the circumstances and the techniques used. (WOW! What colossal BS! Does this claim come with a warranty and money back guarantee?)

What About Assertiveness Training?

It’s true that angry people need to learn to become assertive (rather than aggressive), but most books and courses on developing assertiveness are aimed at people who don’t feel enough anger. (Have we got you trapped yet, into believing that you MUST have some horrible defect that can only be “solved” by psychologists – aka the High Priests of social rules and enforcement?) These people are more passive and acquiescent than the average person; they tend to let others walk all over them. That isn’t something that most angry people do. Still, these books can contain some useful tactics to use in frustrating situations. (See our ads – go to Amazon right now, and buy our useless psycho-Bibles.)

Remember, you can’t eliminate anger—and it wouldn’t be a good idea if you could.(Because, how then, could we exploit and profit from human defects and misery?)In spite of all your efforts, things will happen that will cause you anger; and sometimes it will be justifiable anger. Life will be filled with frustration, pain, loss, and the unpredictable actions of others. You can’t change that; but you can change the way you let such events affect you. Controlling your angry responses can keep them from making you even more unhappy in the long run.

Like this:

Yes, I’m a genetics dummy, but the popular idea that traits such as skin color and eye color are “caused by” a mutation IN ONE PERSON, and that this mutation AT THAT POINT faces a “test” as to whether or not it will spread through a population IS NUTS based on logic alone! There must be two or more individuals who carry a mutation or variation for it to be expressed via reproduction. I have expressed this frustration many times when reading genetics articles and papers. I’m sure that hard core genetic scientists understand this (or maybe not?), but the correct scenario does not make it into presentations that the general population can understand.

Another great post by The Tech Museum of Innovation at Stanford by Dr. Barry Starr:

Get Your Sun

Given all the concern about skin cancer, it can sometimes be easy to forget that sunlight has important benefits too. For example, people need the sun to make their own vitamin D. Nowadays we can (although we don’t always) get enough of this vitamin from our multivitamins, fortified milk, fortified orange juice, etc. But thousands of years ago, we had to rely mostly on the sun.

Which wasn’t a problem in Africa, where we all started out. There is so much sunlight there that getting enough vitamin D wasn’t the problem…the sun’s harsh UV light was. This is why Africans tend to have darker skin.

But getting enough vitamin D was certainly a problem in Northern Europe. As you know if you’ve ever visited there, it is not a place conducive to getting a lot of sun. The winter days are short and the cold weather causes people to cover a lot of their skin and stay indoors. And it is cloudy an awful lot.

Comment: A positive technical adaptation – clothing for cold protection – is counter-adaptational for Vitamin D production. This is rarely mentioned. Technical adaptation, which dominates human “progress” does not “make up for” a lack of natural physical adaptation. When any species of animal or plant moves into new environment, critical adaptations MUST BE MADE. Technical innovation can be fast – fire, new diets, tools, shelter, clothing, but individual physiology remains the same until evolved characteristics can “catch up”- OR NOT. “Change” to the human body has for thousands of years been directed by human-created environments (often degraded and toxic) and less by natural environments.

It should be obvious that technical adaptions do not lead to “better” human bodies, but pose unintended consequences: agriculture, urban living and fossil fuels, while transforming the availability of energy sources for humans, have REQUIRED more and more technical adaptation to compensate for the negative effects they produce. We are “stuck” in a race to overcome the counter-adaptive results of our own innovations, and loosing badly.

It is so hard to get enough sun under these conditions that dark skin is actually a problem. Which is probably why Northern Europeans turned from dark to pale — to get enough vitamin D. This explains the why pretty well but not the how. To understand the how, we need to go over a few basic genetics concepts. Then we’ll see how a trait like fair skin can become common. (A good “Just-So Story)

Bringing Hidden Traits Out

As anyone who looks around knows, people all look pretty different. For the most part, these differences are there because we are all different genetically. Now this doesn’t mean we all have different genes. As humans we all share the same set of genes. What makes each of us different is that we can have different versions of these same genes.

This explains why we’re all different. But it doesn’t do a very good job of explaining how, for example, two darker skinned parents can have a lighter skinned child. To understand this, we need to remember that we have two copies of each of our genes — one from mom and one from dad. What this means is that the same person can have copies of different gene versions.

For example, there is a skin color gene called SLC24A5. This gene comes in two different versions, dark (D) and light (L). People with two dark versions (DD) tend to be much darker than people with two light versions (LL). People with a copy of each (DL) tend to be in between. (Skin color is a spectrum)

Imagine that two DL parents have a child. The child will get one version of the SLC24A5 gene from mom and one from dad. Which copy the child gets from each parent is totally random. So half the time mom will pass a D and half the time an L. Same with dad. This works out to each child having a 1 in 4 chance of getting two L’s and so being much more fair skinned than his or her parents.

That is how Africans can sometimes have a lighter colored child (and, for that matter, a darker one). But now we need to figure out how light colored skin became so common. The answer lies in something called selection.

Pale Skin Sweeps Europe

Imagine a group of Africans migrates to Northern Europe. This population has lots of different gene versions. In terms of skin color, that means that there is a range of colors from dark to darker.

Most of these folks have two dark versions of the SLC24A5 gene — they are DD genetically. But a few might also be DL. These DL people would tend to be on the lighter side of the skin color range.

At some point after coming to Europe, darker skinned people started getting sick. Since most of the people had dark skin, this means that most of the people were sick. This was not a good time to be European. Not only were they sick, but their darker skinned children were too. The kids had weak bones and suffered many problems including an awful disease called rickets.Most of these children didn’t survive to have kids of their own.

Remember, though, that there were a few lighter skinned (or more naked – cold tolerant, or both) ) people who were DL genetically (they had a light version of SLC24A5). They did better because they could get more vitamin D from the weak European sun. And some of the kids inherited their parents’ less dark skin. In the next generation, the people who could go on to have kids were the lighter skinned ones. What this meant was that the relatively rare DL folks could now find each other (sexual selection as well as natural selection) and have kids. Sometimes, both parents would pass an L and make a much lighter skinned child.

These LL people were much better adapted to their surroundings and did better than even their DL neighbors. These LL folks then went on to have kids who would mostly be fair skinned. Repeat this a few times and voila, a pale race is born.

It is important to note here that lack of sun didn’t cause a genetic difference that led to lighter skin. The difference was already there in a few people. It took a pretty brutal selection to rapidly make it the most common skin color gene version in Europeans.

Odds and Ends

This is a nice, clean story. Of course nothing in genetics is so simple. There are always a few twists to keep things interesting.

For example, early results suggest that pale skin swept through Europe between 6,000 and 12,000 years ago (scientists can tell from looking at the DNA around the SLC24A5 gene). But Africans arrived there 30,000-40,000 years ago. So why did it take so long for pale skin to take hold?

One idea is diet. Pale skin swept Europe right around the time that agriculture took hold. The idea is a hunter-gatherer can get enough vitamin D from his or her diet and that a farmer can’t.

These tens of thousands of years in weak sunlight may also have allowed a random change (or mutation) in the SLC24A5 gene to be passed on. In Africa, having fair skin was bad for you. (That is, the “mutation” occurred in Africa thousands of years earlier, NOT when humans moved out of Africa.)In hunter-gatherer Europe, it didn’t much matter (Vitamin D was sufficient in their diet)So a mutation in the SLC24A5 gene might be better tolerated in Europe.

If this were the case, then the original settlers didn’t have a light version of SLC24A5 when they left Africa. It appeared while they were in Europe. (That is, the mutation could have occurred more recently- what matters is that it exists)

Another interesting twist is that SLC24A5 isn’t the only way to end up light skinned.For example, one of the reasons Asians are fair is because of differences in a gene called kitlg.Most likely a few of the settlers of Asia happened to have differences in the kitlg gene. And a few European settlers had differences in the SLC24A5 gene.

Both groups were under the same pressure to become light skinned (which had not changed: Vitamin D is NECESSARY to health, whether or not you live in a high UV environment or a low UV environment.But they responded in different ways based on the genes already within their populations.

Like this:

I’m reposting this because I’m adding a post today on how traits actually appear genetically: mutation is not the only mechanism.

From The Tech museum of innovation, Stanford University (super website)

How Blue Eyed Parents Can Have Brown Eyed Children – Two Different Ways to Get Blue Eyes

This will be the first of two articles on the latest findings on eye color. This one will deal with a plausible way that blue eyed parents might have a brown eyed child. The next one will deal with some of the ways that colors other than green, blue, and brown happen. And a possible reason why more redheads have green eyes.

Eye color is much more complicated than is usually taught in high school (or presented in The Tech’s eye color calculator). There we learn that two genes influence eye color. One gene comes in two versions, brown (B) and blue (b). The other gene comes in green (G) and blue (b). All eye color and inheritance was thought to be explained by this simple model. Except of course for the fact that it is obviously incomplete.

The model cannot, for example, explain how blue eyed parents can have a brown eyed child. Yet this can and does happen (although it isn’t common). New research shows that the first gene is actually two separate genes, OCA2 and HERC2. In other words, there are two ways to end up with blue eyes. Normally this wouldn’t be enough to explain how blue eyed parents can have a brown eyed child. Because of how eye color works (see below), if one gene can cause brown eyes, it would dominate over another that causes blue. In fact, that is what happens with green eyes in the older model. The brown gene dominates over the green one resulting in brown eyes.

The reason these two genes can explain darker eyed kids with lighter eyed parents is that the two genes need each other to work. And that the blue versions are broken genes. Here is what things look like: The key is that if someone makes a lot of pigment in the front part of their eye, they have brown eyes. And if they make none there, they have blue.

Part of the pigment making process involves OCA2 and HERC2. A working HERC2 is needed to turn on OCA2 and OCA2 helps to actually get the pigment made. They need each other to make pigment. So someone with only broken HERC2 genes will have blue eyes no matter what OCA2 says. This is because the working OCA2 can’t be turned on so no pigment gets made. And the opposite is true as well. Someone with broken OCA2 genes will have blue eyes no matter what the HERC2 genes are. Turning on a broken pigment making gene still gives you no pigment. You need a working HERC2 and a working OCA2 to have brown eyes.

Because the two genes depend on each other, it is possible for someone to actually be a carrier of a dominant trait like brown eyes. And if two blue eyed parents are carriers, then they can have a brown eyed child. Genetics is so much fun!

So all you light eyed parents with dark eyed kids, stop asking those paternity questions (unless you have other reasons to be suspicious). Darker eyed kids are a real possibility that can now be explained with real genes.

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Carrying a Dominant Trait PLEASE go to original article for this section – shows diagrams. – Google the article title – the URL is impossible.

Two of the most important genes in eye color are OCA2 and HERC2. Both come in versions that can cause blue eyes. And they need each other to work. (In genetics, a relationship like this is called epistasis.) These two facts provide one explanation for how blue eyed parents can have a brown eyed child. To understand how, a little genetics refresher course is in order.

People have two copies of most of their genes. They get one copy from mom and one copy from dad. These genes can come in different versions (or alleles). For the sake of this discussion, we will say that OCA2 comes in brown (O) and blue (o) versions. Reality is actually a bit more complicated and this will be dealt with in the second article of this series.HERC2 also comes in two different versions, brown (H) and blue (h). Since people have two copies of each gene, there are nine different possible genetic combinations. They are:

These different combinations give the following eye colors:

Looking at the table, it quickly becomes obvious that any time there are two lower case h’s or two lower case o’s, a person has blue eyes. As will be discussed in the next section, this is because HERC2 and OCA2 need each other to have an effect and the blue versions of each gene are broken.

But this part of the article will focus on how two blue eyed parents might have a brown eyed child. Imagine the following blue eyed parents:

The easiest way to figure out what possible eye colors their kids might have is with a Punnett square. The first thing to do in a Punnett square is to array dad’s possible sperm cells across the top of the table and mom’s eggs down the left hand side like this:

Shown below is a simplified version of the table in which duplicate sperm and eggs have been eliminated:

The next step is to fill in the squares with the possible genetic combinations. Filling in the first one immediately gives a brown eyed child:

Here are the rest of the possibilities:

Each child has a 25% chance of having brown eyes and a 75% chance of having blue eyes. This is simplified since the other eye color genes (like those that influence green eyes) are being ignored. But it does mean that brown (or green or hazel or…) eyes are a definite possibility for these blue eyed parents.

Also note that the child in the lower right hand corner no longer carries a brown eye gene. They will not have a brown eyed child as easily as their parents!

And the chances could be even higher with oo HH and OO hh parents. This is what their Punnett square would look like:

All of their kids would have brown eyes! (The table has been simplified to eliminate duplicate gene combinations.) (Also, things are actually a bit more complicated than what I have shown here because HERC2 and OCA2 are so close together on the same chromosome. Go to the end of the article if you’d like to learn what effect this has.)

Again this is understandably a bit confusing since these parents are technically carrying a dominant brown trait. To understand this, we need to get into the nitty gritty of how eye color and these two genes work.

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Why OCA2 and HERC2 Need Each Other

Eye color depends on how much pigment is in the eye. A lot of pigment gives brown, some gives green and little or no gives blue. (Click here to learn why no pigment gives blue.) OCA2 is one of the key genes in determining how much pigment gets made. So it makes sense that if both OCA2 copies are broken, someone would have blue eyes. Because they can’t make a lot of pigment.

Most of the HERC2 gene has very little to do with eye color. There is one small section in the middle, though, that controls whether OCA2 is turned on or not. If this part of HERC2 ends up broken in both copies, then OCA2 can’t get turned on. And if OCA2 is off, no pigment gets made. It is like the OCA2 gene is broken.

Think about OCA2 like a light bulb and HERC2 as a switch. If the light bulb is burned out, it doesn’t matter if the switch is turned on. Just like it doesn’t matter if HERC2 works in someone with broken OCA2. Flipping the switch to a burned out bulb won’t give you any light!

Same thing with a working OCA2 and a broken HERC2. A working light bulb gives no light when the switch is off. And a working OCA2 makes no pigment when the HERC2 gene is broken. This is what happens when blue eyed parents carry a brown eye gene. If they have blue eyes because of a broken HERC2, then they might still have an OCA2 that works. And if they have a broken OCA2, they might have a working HERC2.

Here is how to think of it in terms of these two parents passing on their genes to the next generation:

When these two have kids, one might pass an on switch and the other a working light bulb. Now there is light even though neither parent could make light before. Or in genetic terms, one might pass a working HERC2 and the other a working OCA2. Now there is pigment where there wasn’t any before. The end result is brown eyes.

This light bulb/switch relationship is called epistasis in genetics. This is simply a fancy way of saying that one gene depends on the other. And that if one breaks down, both will no longer have an effect.

So now science can finally explain one mystery of eye color. Or at least propose one of the ways blue eyed parents can have brown eyed kids. The next article will deal with eye colors other than the big three. And talk a bit about why some hair colors tend to have certain eye colors.

OCA2 and HERC2 are Linked

An interesting twist to this puzzle is the fact that HERC2 and OCA2 are so close together on chromosome 15. What this means is that versions tend to travel together. And this affects the combinations of kids that any two parents can actually have.

Imagine these parents:PLEASE go to original article for this section – shows diagrams.

If we assume the OCA2 and HERC2 genes were far from each other, we’d get the following Punnett square:PLEASE go to original article for this section – shows diagrams.

The results are a 9 in 16 chance for brown and a 7 in 16 chance for blue. This assumes that any of four combinations of the two genes is possible. This is true for genes that are far apart or on different chromosomes. This does not tend to be true if genes are really close together like OCA2 and HERC2.

Imagine that these two parent’s chromosomes actually look like the ones on the right. Because of how their alleles (gene versions) happen to be arranged, their real Punnett square would look like this:PLEASE go to original article for this section – shows diagrams.

Now blue is less likely. And all the blue eyed kids wouldn’t be carrying a brown eyed gene anymore! And if the alleles were arranged differently, you’d get different odds.

…Many people become confused at this point … REALLY?

because they think that this situation should happen in every case where two genes are on the same chromosome. It doesn’t because of something called recombination. That is a story for another day…

Like this:

Delightful series of videos from Australia! What happens when “kids” are turned loose in nature – how boys have “grown up” for tens of thousands of years to become “proper” providers and protectors for their families and communities.

Like this:

Study title: Autism, Asperger syndrome and brain mechanisms for the attribution of mental states to animated shapes

What’s wrong with this statement? If you’re an Asperger, it’s obvious: Triangles, animated or static, DO NOT POSSESS MENTAL STATES.

The well-known inability of modern social typicals to distinguish fantasy from physical reality is the core of the problem: ANIMATED SHAPES DO NOT POSSESS MENTAL STATES. TO SEE INTENTION BEHIND “ANIMATED” TRIANGLES IS THE SAME DEFICIT IN MAGICAL THINKING THAT CAUSES SOCIAL TYPICALS TO IDENTIFY DISTANT LIGHTS, PLANETS, STARS and the neighbor’s porch light as UFOS; to see the Virgin Mary on a piece of toast; to believe that God works through online dating services; to assert that coincidences are miracles; to be trapped in that mental stage of childhood in which the universe is a grand puppet show, conjured by supernatural beings to baffle infantile human narcissists. In this cartoon universe, even inanimate objects create critical distortions in perception; distortions that are the product of the self-obsessed human brain.

Ten able adults with autism or Asperger syndrome and 10 normal volunteers(normal is a default condition meaning “not diagnosed ASD”)were PET scanned while watching animated sequences. The animations depicted two triangles moving about on a screen in three different conditions: (1.) moving randomly, (2.) moving in a goal‐directed fashion (chasing, fighting), and (3.) moving interactively with implied intentions (coaxing, tricking).The last condition frequently elicited descriptions in terms of mental states that viewers attributed to the triangles (mentalizing).

The researchers have pre-designated the “illusion” labeled as mentalizing as normal, without questioning their own bias against (vastly more adaptive) accurate perception of reality. Instead, certain humans are pre-judged as pathological for “perceptions” that go beyond typical abilities. Do we label people who can run faster than “normal” as pathological? No; they simply represent the positive tail on the bell curve of human physical ability.

The autism group gave fewer and less accurate descriptions (accuracy = defective perception of reality in modern present-day Homo sapiens)of these latter animations, but equally accurate descriptions of the other animations compared with controls. While viewing animations that elicited mentalizing, in contrast to randomly moving shapes, the normal group showed increased activation in a previously identified mentalizing network (medial prefrontal cortex, superior temporal sulcus at the temporo‐parietal junction and temporal poles). The autism group showed less activation than the normal group in all these regions. However, one additional region, extrastriate cortex, which was highly active when watching animations that elicited mentalizing, showed the same amount of increased activation in both groups. In the autism group this extrastriate region showed reduced functional connectivity with the superior temporal sulcus at the temporo‐parietal junction, an area associated with the processing of biological motion as well as with mentalizing.

This finding suggests a physiological cause for the mentalizing dysfunction in autism: a bottleneck in the interaction between higher order and lower order perceptual processes.

Problem 1: Increased activity is assumed to automatically indicate “better” function, which is an amateur mistake in interpretation. It’s possible (and logical) that increased activity is a neutral state of interest and observation. “Reduced connectivity” could serve to block or dampen immediate irrational interpretation of activity in the environment and allow for analysis of what is actually happening (cause and effect), thus improving outcomes.

Problem 2: The misconceptions due to processing the environment as a supernatural domain that “works” not by natural law, but by magic: “we” are superior beings compared to any living creature, past or present. Possible “modern defects” are automatically considered to be assets…

…Maybe if one is going hunting with Elmer Fudd!

These “researchers” would have us believe that evolution has been working overtime to produce a “superior brain” that can be fooled into mistaking non-living objects as living beings. This is irrational; being fooled is NOT an advantage in activities such as hunting, which require that the hunter is able to discern animals as different to rocks, plants, shadows and imaginary threats caused by sensory distractions. The individual who can “spot” the living creature – and control his or her reactive response (emotion), and ANALYZE whether or not the animal presents a danger or a food opportunity, has a huge advantage. This is especially true given the wildly popular evolutionary strategy of camouflage, mimicry and “copy cat” species in plants and animals.

The inversion of values in mental processing promoted in this (totally unscientific) study is astounding and insulting. To label people who excel at accurate and detailed perception of the environment as “developmentally deficient” is outrageous.

Like this:

Visiting Great Gramma at her farm; that’s me at the far left, looking very awkward and uncomfortable.

I grew up in a family in which mental illness was a fact of life. I’m Asperger (a valid brain type from my POV) and bipolar. My brother was schizoid. Everyone functioned – not great, but well enough, but I was the only one who actively searched for answers and treatment. It caused a rift in the family and I was essentially kicked out for wanting to be healthy. I would see my brother suffering, but he refused all treatment, even when he began to get into trouble with authorities and help was offered. It is incomprehensible to me why a person would want to stay in a frightening and agitated state and not want to live as well as possible. But then, I observe the lives of so-called normal people and think the same thing. It’s difficult for me to remember that I once had a family, so great was the gulf between my expectations and theirs. From a young age I began building a “ghost” family of artists and writers whom I admired through their works, and from landscapes and buildings in the environment, which is populated by thousands of strangers as well as friends. The habit became so rewarding that I just kept it up, accumulating a complex library of rich characters and environments that never leaves me. This creative act is likely to be the result of being a visual thinker.

Most everyone, especially when young, asks, Who am I? The answer for me turned out to be simple: I am everything I have ever seen.

Earliest humans had diverse range of body types, just as we do today (title is a bit misleading)

New research harnessing fragmentary fossilssuggests our genus has come in different shapes and sizes since its origins over two million years ago, and adds weight to the idea that humans began to colonize Eurasia while still small and lightweight.

“If someone asked you ‘are modern humans 6 foot tall and 70kg?’ you’d say ‘well some are, but many (most) people aren’t,’* and what we’re starting to show is that this diversification happened really early in human evolution,” said Stock.

*This is a welcome observation, But breathtakingly obvious! DUH! Buyer beware; this research is heavily “engineered” and actually doesn’t add anything new.

Human body has gone through four stages of evolution

Research into 430,000-year-old fossils collected in northern Spain (Atapuerca) found that the evolution of the human body’s size and shape has gone through four main stages

“This is really interesting since it suggeststhat theevolutionary process in our genus is largely characterized by stasis (i.e. little to no evolutionary change) in body formfor most of our evolutionary history,” wrote Quam.

Analysis of nuclear DNA from Sima de los Huesos hominins provides evidence of their relationship to Neanderthals

March 15, 2016, Max-Planck-Gesellschaft

Summary:

Previous analyses of the hominins from Sima de los Huesos in 2013 showed that their maternally inherited mitochondrial DNA was distantly related to Denisovans, extinct relatives of Neanderthals in Asia. This was unexpected since their skeletal remains carry Neanderthals-derived features. Researchers have since worked on sequencing nuclear DNA from fossils from the cave, a challenging task as the extremely old DNA is degraded to very short fragments. The results now show that the Sima de los Huesos hominins were indeed early Neanderthals.

Like this:

One of the most annoying Asperger misbehaviors is “Unusual preoccupations or rituals: A child with Asperger’s syndrome may develop rituals that he or she refuses to alter, such as getting dressed in a specific order.”

Does this mean that neurotypical children are encouraged to put on articles of clothing and accessories in a different order each day? Why then do we teach children a “getting dressed” ritual, among many other rituals?

And why in this video do the monkey children not wear underwear? Very odd.